S-Equol in Alzheimer's Disease (SEAD) Trial

Alzheimer's disease (AD) is a progressive brain disorder which causes memory and thinking problems. The exact cause of AD is unknown. Researchers believe mitochondria (the part of your cells that produces energy) might be linked to symptoms of AD. Some studies have shown that patients with Alzheimer's disease have reduced mitochondrial activity or have fewer mitochondria present in neurons. In this study, it is believed that by targeting mitochondria, we might learn more about its influence on AD symptoms.

Mitochondria have a receptor site for estrogen (a hormone) called estrogen receptor β (ERβ). When estrogen attaches to this site, it promotes mitochondrial function. Studies have also suggested ERβ stimulation can cause cells to create new mitochondria. More mitochondria, or increased activity of existing mitochondria, in the cell might have an impact on patients with Alzheimer's disease. One way to measure this increase in function is to look for the presence of an enzyme called COX in your blood. If a drug increases mitochondrial function, there will be an increase in COX concentration in the bloodstream.

By doing this study we hope to learn if S-equol, a compound that acts like estrogen in the body, causes such an increase in mitochondrial activity. We also hope to determine the tolerability of a therapeutic dose of S-equol. It is our goal to advance the understanding of AD, particularly in women.

Inclusion criteria

• Very mild (CDR 0.5) or mild (CDR 1) AD at time of last KU ADC assessment
• Have a study partner
• Speak English as primary language

Exclusion criteria

• No viable study partner
• Report a potentially confounding, serious medical risk such as type 1 diabetes, cancer, or a recent cardiac event (i.e. heart attack, angioplasty, etc.)
• Use any type of estrogen replacement therapy